Cirrhosis
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Cirrhosis
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Cirrhosis
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Alcoholic cirrhosis p. 69, 400
cholelithiasis and p. 405
Alcoholism p. 595
cirrhosis and p. 398
Amenorrhea
cirrhosis p. 398
Anemia
cirrhosis p. 398
Anorectal varices
cirrhosis as cause p. 398
Ascites
cirrhosis p. 398
Asterixis p. 80, 537
cirrhosis p. 398
Cirrhosis p. 398
α1-antitrypsin deficiency p. 401
alcoholic p. 69, 400
bacterial peritonitis (spontaneous) p. 399
cholelithiasis and p. 405
cystic fibrosis p. 58
encephalopathy with p. 400
esophageal varices and p. 386
fructose intolerance p. 78
granulomatous disease p. NaN
gynecomastia p. 673
hemochromatosis p. 404
hepatocellular carcinomas p. 401
hyperbilirubinemia in p. 402
loop diuretics for p. 632
non-alcoholic fatty liver disease p. 400
pleural effusion p. 705
portal hypertension p. 398
serum markers for p. 399
Wilson disease p. 404
Edema (generalized)
cirrhosis p. 398
Gynecomastia p. 673
cirrhosis p. 398
Hepatic cirrhosis p. 705
Hepatic encephalopathy p. 400
cirrhosis p. 398
Hepatitis
cirrhosis p. 398
Hepatocellular carcinomas p. 401
cirrhosis and p. 398
“Hobnail” liver in alcoholic cirrhosis p. 400
Hyperbilirubinemia
cirrhosis and p. 398
Hypoalbuminemia
alcoholic cirrhosis as cause p. 400
Hyponatremia p. 615
cirrhosis and p. 398
Jaundice p. 402
alcoholic cirrhosis and p. 401
cirrhosis p. 398
Liver disease
cirrhosis p. 69, 78
Peripheral edema
cirrhosis and p. 398
Petechiae
with cirrhosis p. 398
Portal hypertension p. 398
cirrhosis and p. 398
Purpura
cirrhosis p. 398
Spider angiomas
cirrhosis p. 398
Splenomegaly
cirrhosis p. 398
Testicular atrophy
cirrhosis p. 398
Thrombocytopenia p. 415
cirrhosis p. 398
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When cells are injured or damaged and die off, usually that dead tissue that was previously full of living cells becomes fibrotic, meaning it becomes thickened with heaps and heaps of protein and forms scar tissue.
So when your liver is constantly forced to process alcohol like in alcoholic liver disease, or subject to a viral attack for a long time like in HBV, or anything else that causes a long-term or chronic state of liver cell or hepatocyte destruction and inflammation, your liver can become seriously scarred and damaged to the point where it’s no longer reversible, at which point it becomes fibrotic and in the liver we call this process cirrhosis.
Because it’s usually irreversible, cirrhosis is often referred to as “end-stage” or “late-stage” liver damage.
When liver cells are injured, they start to come together and form what are called regenerative nodules. You can think of these as colonies of living liver cells. These are one of the classic signs of cirrhosis and are why a cirrhotic liver is more bumpy as opposed to a smooth, healthy liver.
Also with cirrhotic liver tissue, you’ll see that in between these clumps of cells or nodules, is fibrotic tissue and collagen.
Here’s a classic histology image of cirrhotic tissue, this clump of cells in the middle is the regenerative nodule, and these blue stains surrounding it are the bands of protein from the process of fibrosis.
If we zoom out a bit and look at it with the naked eye, we’ll again see these nodules, which have fibrotic protein bands in between.
How do these bands of fibrotic tissue form though? Well fibrosis is a process mediated by special cells called stellate cells, that sit between the sinusoid and hepatocyte, known as the perisinusoidal space.
Here’s a pretty basic layout of the basic functional unit of the liver, you’ve got the portal vein and hepatic artery that combine into a sinusoid, which then goes into the central vein, and these are all lined with hepatocytes.
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